ZFIN ID: ZDB-PUB-961014-374
Analysis of FGF function in normal and no tail zebrafish embryos reveals separate mechanisms for formation of the trunk and the tail
Griffin, K., Patient, R., and Holder, N.
Date: 1995
Source: Development (Cambridge, England)   121: 2983-2994 (Journal)
Registered Authors: Griffin, Kevin, Holder, Nigel, Patient, Roger K.
Keywords: none
MeSH Terms:
  • Animals
  • DNA-Binding Proteins/physiology
  • Fetal Proteins/physiology
  • Fibroblast Growth Factors/physiology*
  • Gastrula/physiology*
  • Gene Expression Regulation, Developmental*
  • In Situ Hybridization
  • Mesoderm/physiology
  • Models, Genetic
  • Morphogenesis/genetics
  • Phenotype
  • T-Box Domain Proteins*
  • Tail/embryology
  • Zebrafish/embryology*
  • Zebrafish/genetics
PubMed: 7555724
To analyse the roles of FGF activity and brachyury during gastrulation we have directly compared the consequences of inhibition of FGF-receptor signalling with the phenotype of the zebrafish brachyury mutant, no tail (ntl). We show that expression of ntl is regulated by FGF and that inhibition of FGF receptor-signalling leads to complete loss of the trunk and tail. Since the ntl mutant lacks the tail and notochord but has an otherwise normal trunk, this demonstrates that trunk development is dependent upon an unidentified gene, or set of genes, referred to as no trunk (ntk) which is regulated by FGF. We propose a model to explain the FGF-dependent regulation of ntl and ntk that accounts for the above phenotypes. Consistent with this model, over-expression of eFGF led to suppression of anterior fates and development of trunk and tail derivatives only. In addition, widespread activation of convergence and extension movements resulted in the formation of multiple axis- like structures. Expression of eve1 and cad1 was also regulated by FGF activity, suggesting that during gastrulation FGF activity is normally restricted to the germ ring where these genes, and ntl, are expressed. Taken together these data suggest that the germ ring acts as a posteriorising centre during AP patterning, mediated by FGF activity in this tissue.